Thyrotropin-releasing hormone (TRH) increases prolactin release and synthesis, but the analog specificities for the two processes are not the same, using either GH-cells which are rat pituitary cells on culture, or normal pituitary cells in culture. We will investigate analogs of TRH which show greater specificity for release or synthesis. We will determine whether TRH binds at two physically distinct sites to cause the two processes or if it causes two separate interactions at one site. We will investigate analogs of TRH which may distinguish between prolactin and thyrotropin release. We will examine the effects of chronic treatment with bromocriptine to see if bromocriptine causes degradation of prolactin in systems other than in monolayer culture, to determine if degradation of prolactin completely accounts for decreased prolactin accumulation or if a change in synthesis is involved as well. We will see by what mechanisms prolactin is degraded and if degradation is independent of or secondary to an inhibition of release. We will determine if bromocriptine and estrogen have direct effects on cell growth. We will investigate the mechanisms by which bromocriptine causes the acute inhibition of prolactin release and how estrogen makes the cells less sensitive to bromocriptine. We will attempt to get pure populations of prolactin producing cells in culture.